By P. Dörmer (auth.), Prof. Dr. T. Büchner, Prof. Dr. G. Schellong, Prof. Dr. W. Hiddemann, Prof. Dr. J. Ritter (eds.)

Acute leukemia a really homogenous disorder didn't holiday throughout the sound barriere of while untreated finds a considerable hetero­ unsatisfactory treatment premiums even in distinct sub­ geneity in its reaction to treatment. whereas therapy teams. whereas new protocols together with extra is completed in a undeniable percentage of pa­ powerful supportive care express a few elevate tients different circumstances turn out to be hugely resis­ within the preliminary reaction premiums and likely im­ tant. The curability is better in acute provements within the long term effects, no ben­ lymphoblastic (ALL) than in acute myeloid eficial influence at the relapse fee throughout the (AML) leukemia and - inside of either kind- first 1 Y2 years emerged from any of those greater in little ones in comparison to adults. regimens. therefore, excessive percentages for treatment are the 2 age teams and phone varieties may be shortly limited to young children with ALL extra subdivided into prognostic teams and to lesser proportions teenagers with through detailed diagnostic positive factors. therefore, in AML and adults with ALL and AML.

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Additional info for Acute Leukemias II: Prognostic Factors and Treatment Strategies

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Identical mutations at both stages, 2. acquisition of a point mutation at relapse, or 3. absence of a mutated alleles, initially characterizing leukemic blasts (Fig. 3). Ras gene muations can obviously occur at various stages during the evolution of AML. Fig. 3. Detection of mutated N-ras codon 12 ane1es in two AML patients investigated at initial diagnosis (1. 4), remission (2, 5), and relapse (3, 6). DNA preparations obtained from peripheral blood samples were amplified by peR and screened using oligonucleotide probes specific for the wild-type N-ras 12-sequence GGT (glycine) as wen as mutation AGT (serine), or TGT (cysteine).

2. Sequential observations of cell kinetics in a case with RA. e, blast frequency/tOO bone marrow cells (BMC); 0, blast S-phase frequency /1000 BMC; &, myeloid maturation index Fig. 3. Sequential observations of cell kinetics in a case initially presenting with RAEB. Although the FAB subgroup changed severalfold due to varying BM blast cell counts, there was no indication of leukemia development at any time. For symbols, see legend to Fig. 1 ............ 3 Fig. 4. Sequential observations of cell kinetics in a case with RAEB gradually progressing to overt AML.

Recently, molecular genetic approaches have complemented these investigations. In this chapter we briefly discuss some clinical applications or recombinant DNA strategies as powerful tools for the identification and monitoring of clonal cell populations in hematopoietic neoplasias. Gene Rearrangements at Chromosomal Breakpoints A novel set of clonal markers has been obtained through the molecular cloning of breakpoints involved in tumor-specific chromosomal aberrations. A case in point is the Philadelphia translocation (Ph) observed in more than 95% of chronic myelocytic leukemias (CMLs) and 20% of adult acute lymphoblastic leukemias (ALLs).

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